Sympathetic nervous system-mediated fibro-adipogenic progenitor mobilization drives stroke-related sarcopenia.
Overview
13 affiliations
- Department of Endocrinology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong China
- Center for Stem Cell Biology and Tissue Engineering, Key Laboratory for Stem Cells and Tissue Engineering, Ministry of Education, Sun Yat-sen University, Guangzhou, Guangdong China
- National-Local Joint Engineering Research Center for Stem Cells and Regenerative Medicine, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong China
- Department of Critical Care Medicine, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong China
- Department of Surgery Intensive Care Unit, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong China
- Department of General Intensive Care Unit, Lingnan Hospital, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong China
- Department of Rehabilitation Medicine, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong China
- Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong China
- Department of Gastrointestinal Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong China
- Department of Anesthesiology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong China
- Department of Medical Ultrasonics, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou Guangdong, China
- Scientific Research Center, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong China
- Department of Histoembryology and Cell Biology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong China
Abstract
Patients who survive stroke usually experience rapid muscle wasting and an increased risk of physical disability. Although multifactorial interactions, including malnutrition, disuse, systemic catabolic imbalance, and neurohormonal dysregulation, are thought to contribute to the progression of stroke-related sarcopenia, the underlying mechanisms of this brain–muscle crosstalk remain elusive. Muscle-resident fibro-adipogenic progenitors (FAPs) are indispensable for maintaining muscle homeostasis and function as initial sensors of external perturbations. In the present study, we report that FAPs rapidly respond to the overactive sympathetic nervous system (SNS) and egress from the muscle niche into circulation during the acute phase of stroke. FAP-specific ablation of adrenoceptor beta 2 (Adrb2) markedly ameliorated stroke-related sarcopenia, highlighting the central role of SNS-mediated FAP loss in its pathogenesis. Mechanistically, increased norepinephrine release initiates FAP mobilization through the activation of pro-migratory signals and the degradation of extracellular matrix components. Using transcriptomic profiling, we further characterized insulin growth factor-1 (IGF-1) as a key anti-atrophic executive factor predominantly derived from FAPs. Collectively, our work demonstrates that the SNS-mediated loss of FAPs and subsequent compromised IGF-1 secretion contribute to sarcopenia in mice following stroke. Targeting this mechanism by early anti-sympathetic treatment with propranolol may effectively restore muscle homeostasis and mass after stroke.
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- geo:GSE49910, at NCBI GEO; found in the text, “Stroke mobilizes the egress of FAPs from…”
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 25 authors, 2 keywords, 1 funder, 83 references.
Cite
This paper
Huang, Y., Liu, Y., Li, R., Fan, M., Liu, Y., Wang, Y., Sui, X., Yuan, X., Lu, Q., Qiu, Y., Li, R., Chen, J., Zhang, B., Liu, S., Ou, C., Ma, Y., Lai, X., Ren, J., Lu, Z., . . . Xiang, A. P. (2026). Sympathetic nervous system-mediated fibro-adipogenic progenitor mobilization drives stroke-related sarcopenia. Cell discovery, 12(1), 49. https://
BibTeX
@article{huang2026sympat
author = {Huang, Yinong and Liu, Yilin and Li, Ruijie and Fan, Mingming and Liu, Yixuan and Wang, Yiling and Sui, Xin and Yuan, Xiaofeng and Lu, Qiying and Qiu, Yuan and Li, Ruijun and Chen, Jierui and Zhang, Bingjun and Liu, Sanxin and Ou, Chuyun and Ma, Yuanchen and Lai, Xiaofan and Ren, Jie and Lu, Zhengqi and Yi, Huimin and Huang, Weijun and Wang, Jiancheng and Li, Yanbing and Xiao, Haipeng and Xiang, Andy Peng},
title = {{Sympathetic nervous system-mediated fibro-adipogenic progenitor mobilization drives stroke-related sarcopenia}},
journal = {Cell discovery},
year = {2026},
month = jul,
volume = {12},
number = {1},
pages = {49},
publisher = {Nature Publishing Group},
issn = {2056-5968},
doi = {10.1038/
url = {https://
pmid = {42409779},
pmcid = {PMC13338466}
}
RIS
TY - JOUR
AU - Huang, Yinong
AU - Liu, Yilin
AU - Li, Ruijie
AU - Fan, Mingming
AU - Liu, Yixuan
AU - Wang, Yiling
AU - Sui, Xin
AU - Yuan, Xiaofeng
AU - Lu, Qiying
AU - Qiu, Yuan
AU - Li, Ruijun
AU - Chen, Jierui
AU - Zhang, Bingjun
AU - Liu, Sanxin
AU - Ou, Chuyun
AU - Ma, Yuanchen
AU - Lai, Xiaofan
AU - Ren, Jie
AU - Lu, Zhengqi
AU - Yi, Huimin
AU - Huang, Weijun
AU - Wang, Jiancheng
AU - Li, Yanbing
AU - Xiao, Haipeng
AU - Xiang, Andy Peng
TI - Sympathetic nervous system-mediated fibro-adipogenic progenitor mobilization drives stroke-related sarcopenia
T2 - Cell discovery
J2 - Cell Discov
PY - 2026
DA - 2026/
VL - 12
IS - 1
SP - 49
SN - 2056-5968
PB - Nature Publishing Group
DO - 10.1038/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1038/
"type": "article-journal",
"title": "Sympathetic nervous system-mediated fibro-adipogenic progenitor mobilization drives stroke-related sarcopenia",
"container-title": "Cell discovery",
"author": [
{
"family": "Huang",
"given": "Yinong"
},
{
"family": "Liu",
"given": "Yilin"
},
{
"family": "Li",
"given": "Ruijie"
},
{
"family": "Fan",
"given": "Mingming"
},
{
"family": "Liu",
"given": "Yixuan"
},
{
"family": "Wang",
"given": "Yiling"
},
{
"family": "Sui",
"given": "Xin"
},
{
"family": "Yuan",
"given": "Xiaofeng"
},
{
"family": "Lu",
"given": "Qiying"
},
{
"family": "Qiu",
"given": "Yuan"
},
{
"family": "Li",
"given": "Ruijun"
},
{
"family": "Chen",
"given": "Jierui"
},
{
"family": "Zhang",
"given": "Bingjun"
},
{
"family": "Liu",
"given": "Sanxin"
},
{
"family": "Ou",
"given": "Chuyun"
},
{
"family": "Ma",
"given": "Yuanchen"
},
{
"family": "Lai",
"given": "Xiaofan"
},
{
"family": "Ren",
"given": "Jie"
},
{
"family": "Lu",
"given": "Zhengqi"
},
{
"family": "Yi",
"given": "Huimin"
},
{
"family": "Huang",
"given": "Weijun"
},
{
"family": "Wang",
"given": "Jiancheng"
},
{
"family": "Li",
"given": "Yanbing"
},
{
"family": "Xiao",
"given": "Haipeng"
},
{
"family": "Xiang",
"given": "Andy Peng"
}
],
"container-title-short":
"volume": "12",
"issue": "1",
"page": "49",
"DOI": "10.1038/
"PMID": "42409779",
"PMCID": "PMC13338466",
"ISSN": "2056-5968",
"publisher": "Nature Publishing Group",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
7,
7
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1038/s41467-026-72823-9
- Catecholaminergic neurons boost fibroblast osteogenic activity in keloid.Journal: Nature communicationsIn common: cellular / molecular, 2 references
- [2] doi:10.1038/s41467-026-74038-4 [code]
- Semaglutide attenuates neuroinflammation in male mice.Journal: Nature communicationsIn common: cellular / molecular, 2 references
- [3] doi:10.1016/j.isci.2026.115779
- Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/
NLRP3 pathway. Journal: iScienceIn common: stroke, cellular / molecular, 1 reference - [4] doi:10.1093/braincomms/fcag322 [code]
- Genomic insights into stroke recovery: cross-phenotype associations.Journal: Brain communicationsIn common: stroke, 1 reference
- [5] doi:10.1038/s43587-026-01204-0
- Fibronectin mediates APOE4-driven blood-brain barrier dysfunction in Alzheimer's disease.Journal: Nature agingIn common: cellular / molecular, 1 reference
- [6] doi:10.1172/jci197345
- Catecholamine-mediated release of miR-133a-3p from adipocytes regulates the onset of chronic primary pain.Journal: The Journal of clinical investigationIn common: cellular / molecular, 1 reference
- [7] doi:10.1126/sciadv.aeb7558
- An engineered insulin analog with dual insulin and IGF-1 receptor agonism and distinct signaling.Journal: Science advancesIn common: cellular / molecular, 1 reference
- [8] doi:10.1038/s41467-026-71643-1 [code]
- Pericytes are organ-specific regulators of tissue morphogenesis.Journal: Nature communicationsIn common: cellular / molecular, 1 reference
- [9] doi:10.1007/s10571-026-01743-5 [code]
- Adapted Smart-seq3xpress Facilitates Selective Microglial Transcriptomic Profiling From Frozen Brain Tissue.Journal: Cellular and molecular neurobiologyIn common: stroke, cellular / molecular, 1 reference
- [10] doi:10.1038/s41598-026-51310-7
- BTK promotes neuroinflammation after intracerebral hemorrhage involving hub genes and alterations in microglial functions.Journal: Scientific reportsIn common: stroke, cellular / molecular, 1 reference
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.
